The kidney in hantavirus infection—epidemiology, virology, pathophysiology, clinical presentation, diagnosis and management

Abstract

Hantavirus-induced diseases are emerging zoonoses with endemic appearances and frequent outbreaks in different parts of the world. In humans, hantaviral pathology is characterized by the disruption of the endothelial cell barrier followed by an increased capillary permeability, thrombocytopenia due to platelet activation/depletion and an overactive immune response. Genetic vulnerability due to certain human leukocyte antigen haplotypes is associated with disease severity. Typically, two different hantavirus-caused clinical syndromes have been reported: haemorrhagic fever with renal syndrome (HFRS) and hantavirus cardiopulmonary syndrome (HCPS). The primarily affected vascular beds differ in these two entities: renal medullary capillaries in HFRS caused by Old-World hantaviruses and pulmonary capillaries in HCPS caused by New-World hantaviruses. Disease severity in HFRS ranges from mild, e.g., Puumala-virus associated nephropathia epidemica, to moderate, e.g., Hantaan- or Dobrava-virus infections. HCPS leads to a severe acute respiratory distress syndrome with high mortality rates. Due to novel insights into organ tropism, hantavirus-associated pathophysiology and overlapping clinical features HFRS and HCPS are believed to be interconnected syndromes frequently involving the kidneys. As there are no specific antiviral treatments or vaccines approved in Europe or the United States, only preventive measures and public awareness may minimize the risk of hantavirus infection. Treatment remains primarily supportive and, depending on disease severity, more invasive measures (e.g., renal replacement therapy, mechanical ventilation and extracorporeal membrane oxygenation) are needed.

RNA transcriptome analysis of platelets revealed altered platelet responses and the mechanism of thrombocytopenia in SFTS

“…In addition to playing a central role in hemostasis, platelets participate in regulating the immune response against infection with viruses such as DENV, Hantavirus, and SARS-CoV-2 [19,38]. Here, we investigated the platelet response to SFTSV infection based on the transcriptome data of platelets puri ed from SFTS patients and revealed the functional platelet alterations.…”

“…Human infection with hemorrhagic fever disease-associated viruses (HFVs), such as Crimean-Congo hemorrhagic fever virus (CCHFV), Hantaan virus, Ebola virus, and Lassa virus, can lead to thrombocytopenia, resulting in severe bleeding in patients [18][19][20][21]. Thrombocytopenia induced by infection with the above mentioned HFVs was found to occur via four main mechanisms, including destruction of platelets by direct interaction with virus, immunological destruction of platelet-virus complexes, impairment of megakaryocytes and progenitor cells to produce platelets, and inhibition of platelet function [22].…”

Hantavirus Diseases – A Comprehensive Review

“…Atypical conjunctival haemorrhages and fine petechiae are often seen on the palate near the conclusion of the febrile phase. The hypertensive phase can last for up to two days [13]. Hypotension and shock may be seen in severe cases.…”

Hemorrhagic fever viruses: Pathogenesis, therapeutics, and emerging and re-emerging potential

“…HFVs are transmitted through contact with or inhalation of contaminated materials from animal reservoirs or arthropod vectors; however, human-to-human spread through contact with infected blood and other body fluids is possible for most HFVs ( Marty et al, 2006 ; Koehler et al, 2022 ). The incubation period varies from 2 to 35 days and begins with a prodromal period that typically last less than 1 week.…”

“…The incubation period varies from 2 to 35 days and begins with a prodromal period that typically last less than 1 week. This phase is followed by an increase in viral replication, which leads to an excessive release of cytokines, causing endothelial activation, increased vascular permeability, vasodilatation with subsequent hypotension, multiorgan failure, and death ( Marty et al, 2006 ; Koehler et al, 2022 ).…”